Identification of FOXC1 as a TGF-β1 Responsive Gene and Its Involvement in Negative Regulation of Cell Growth

Zhou, Yong; Kato, Hidenori; Asanoma, Kazuo; Kondo, Haruhiko; Arima, Takahiro; Kato, Kiyoko; Matsuda, Takao; Wake, Norio

doi:10.1006/geno.2002.6860

Cited by 48 publications

(44 citation statements)

References 29 publications

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“…Mutations in this gene cause various glaucoma phenotypes including primary congenital glaucoma, autosomal-dominant iridogoniodysgenesis anomaly, and Axenfeld-Rieger anomaly (44). There is evidence that FOXC1 functions as a tumor suppressor through transforming growth factor-h1 -mediated signals (45), and the FOX gene family is highly implicated in carcinogenesis (46).…”

Section: Discussionmentioning

confidence: 99%

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The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

Oppenheimer¹,

Cheung²,

Gerald

2007

Molecular Cancer Therapeutics

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Section: Discussionmentioning

confidence: 99%

“…RET mutations have not been identified in neuroblastic tumors (53). In rodent embryonic and adult tissues, RET is highly expressed in the enteric, sympathetic, sensory, central motor, dopamine, and adrenergic neurons, suggesting its involvement in the differentiation and survival of these neurons (45).…”

Section: Discussionmentioning

confidence: 99%

The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

Oppenheimer¹,

Cheung²,

Gerald

2007

Molecular Cancer Therapeutics

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“…It has transcriptional activator domains at the ends of the molecule and has an inhibitory/phosphorylation domain in the central region (Berry et al, 2002). Several studies have suggested its expression may be regulated by TGF␤ signaling Zhou et al, 2002;Mattiske et al, 2006). Here we have made three further advances in our understanding of FoxC1 biology, specifically regarding its regulation, its target genes, and its function in the development of the mesoderm germ layer.…”

Section: Discussionmentioning

confidence: 99%

The role of FoxC1 in early Xenopus development

Birsoy

Kofron

et al. 2007

Developmental Dynamics

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FoxC1 is an important transcription factor in vertebrate development since its mutation in humans results in Axenfeld-Rieger syndrome. In the mouse, disturbance of its function causes congenital hydrocephalus and abnormalities in the development of various mesodermal derivatives. In this report, we provide one mechanistic basis for the requirement for FoxC1 in vertebrate development. We find that, in Xenopus laevis embryos, FoxC1 expression is regulated by the maternal T-box transcription factor VegT, via the nodal sub-family of TGF␤ signaling transducers. We show that at the late neurula to early tailbud stage, FoxC1 depletion causes the down-regulation of adhesion molecules, EP and E cadherin, as well as members of the Ephrin/EphR signaling families in the mesoderm germ layer resulting in the loss of adhesion and apoptosis of mesodermal cells. Developmental Dynamics 236:2731-2741, 2007.

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“…However, lack of FoxC1 expression yielded improper PAA remodeling, resulting in interruption or coarctation of the aortic arch (Winnier et al, 1999). TGF-␤ upregulates FOXC1 transcription in several human cancer cell lines and ectopic expression of FOXC1 cDNA in HeLa cells, which lack both copies of the FOXC1 allele, restores the potential of TGF-␤1 to inhibit cell growth (Zhou et al, 2002). Therefore, FOXC1 is a TGF-␤-responsive gene, and failure of CNCCs in the OFT of Ltbp1L mutants to express FoxC1 might be a consequence of decreased Tgf-␤ signaling.…”

Section: Research Articlementioning

confidence: 99%

Long form of latent TGF-β binding protein 1 (Ltbp1L) is essential for cardiac outflow tract septation and remodeling

et al. 2007

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Latent TGF-β binding protein 1 (LTBP1) is a member of the LTBP/fibrillin family of extracellular proteins. Due to the usage of different promoters, LTBP1 exists in two major forms, long (L) and short (S), each expressed in a temporally and spatially unique fashion. Both LTBP1 molecules covalently interact with latent TGF-β and regulate its function,presumably via interaction with the extracellular matrix (ECM). To explore the in vivo role of Ltbp1 in mouse development, at the time when only the L isoform is expressed, we mutated the Ltbp1L locus by gene targeting. Ltbp1L-null animals die shortly after birth from defects in heart development, consisting of the improper septation of the cardiac outflow tract(OFT) and remodeling of the associated vessels. These cardiac anomalies present as persistent truncus arteriosus (PTA) and interrupted aortic arch(IAA), which are associated with the faulty function of cardiac neural crest cells (CNCCs). The lack of Ltbp1L in the ECM of the septating OFT and associated vessels results in altered gene expression and function of CNCCs and decreased Tgf-β activity in the OFT. This phenotype reveals a crucial role for Ltbp1L and matrix as extracellular regulators of Tgf-β activity in heart organogenesis.

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Identification of FOXC1 as a TGF-β1 Responsive Gene and Its Involvement in Negative Regulation of Cell Growth

Cited by 48 publications

References 29 publications

The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

The role of FoxC1 in early Xenopus development

Long form of latent TGF-β binding protein 1 (Ltbp1L) is essential for cardiac outflow tract septation and remodeling

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